Effect of ADH, aldosterone, ouabain, and amiloride on toad bladder epithelial cells

Handler, Jerome S.; Preston, AS; Orloff, Jack

doi:10.1152/ajplegacy.1972.222.5.1071

Cited by 93 publications

(45 citation statements)

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“…Aldosterone is believed to act on tight epithelia by enhancing the Na+ permeability of the apical membrane (Handler, Preston & Orloff, 1972). In Fig.…”

Section: Effect Of Aldosteronementioning

confidence: 99%

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Eaton¹

1981

The Journal of Physiology

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SUMMARY1. Intracellular potentials and the intracellular activities of Na+ and K+ were examined using conventional and ion-selective micro-electrodes.2. In animals on a normal diet, the intracellular Na+ activity was 8-6 + 2-9 mM (mean + S.D.) with a mean short-circuit current of 2-8 + 09 ,uA/cm2.3. In animals on a low-Na+ diet, the intracellular Na+ activity was 185 + 9-9 mM with a short-circuit current of 4-5+13 ItA/cm2 (mean+ S.D.).4. There was a correlation between short-circuit current and intracellular Na+ activity which could be fitted by a saturating hyperbolic relationship.5. Treatment of the tissue with ouabain and amiloride produced an increase and a decrease, respectively, in the intracellular Na+ activity.6. Treatment with aldosterone produced a large increase in short-circuit current with a substantial increase in intracellular Na+ activity.7. Intracellular Na+ activity does not seem to affect apical membrane permeability directly.

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“…Aldosterone is believed to act on tight epithelia by enhancing the Na+ permeability of the apical membrane (Handler, Preston & Orloff, 1972). In Fig.…”

Section: Effect Of Aldosteronementioning

confidence: 99%

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Eaton¹

1981

The Journal of Physiology

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“…In discussing the mechanism of action of aldosterone on transport, it is customary to think of the hormone as having either a "permeability" effect (1,(3)(4)(5)(6) or an "energetic" effect (2) or both (11,12). For H+ transport, using the familiar equivalent circuit, we found previously that the conductance in the active pathway is increased (13).…”

Section: Resultsmentioning

confidence: 99%

Effect of aldosterone on the coupling between H+ transport and glucose oxidation.

Al‐Awqati¹

1977

J. Clin. Invest.

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A B S T R A C T The mode of action of aldosterone on the energetics of H+ transport in the turtle bladder was examined with the rate of glucose oxidation as an index of the metabolic activity of the epithelium (we show that H+ transport is not coupled to fatty acid oxidation).Within 6 h of addition of aldosterone H+, transport increased; so did glucose oxidation. The amount of H+ transport per mole of 14CO2 produced from glucose oxidation was 15.6 eq mol-' in the control hemibladder, while in the aldosterone-treated bladder it was 13.6, A = 2.0+4.0 (n = 6). However, in bladders exposed to aldosterone for 20 h, the relation oftransport to glucose oxidation was significantly altered: control 10.8, aldosterone 16.4, A = 4.5+2.5, P < 0.02, ni = 7. The slope of H+ transport on the applied electrochemical gradient was steeper during both short-and long-term incubations. However, the maximum gradient necessary to nullify the net rate of secretion was unaltered in both experiments. Evidence is presented that aldosterone does not alter the passive backflux into the cell. In five additional experiments where aldosterone produced no significant stimulation of H+ transport, no change was noted in any of the metabolic or transport characteristics measured, suggesting that the alterations discussed above are dependent on the stimulation of H+ transport by the hormone.These results, along with some thermodynamic considerations, suggest that the effect of aldosterone is primarily exerted on the transport process rather than on metabolism. Further, it appears that prolonged stimulation of transport work leads to secondary alterations in the metabolic pathways reminiscent of the changes that occur in skeletal muscles of athletes undergoing physical conditioning.

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“…First, the serum factor inhibits transepithelial sodium transport by the anuran bladder, and the urine factor, if it is the same substance, should have similar inhibitory capabilities. Second, isolated epithelial cells removed from the intact toad bladder have been used recently to investigate the site of action of inhibitors of sodium transport (7). Inhibitors that act at the serosal surface of the epithelia (e.g.…”

Section: Introductionmentioning

confidence: 99%

“…Inhibitors that act at the serosal surface of the epithelia (e.g. ouabain) increase intracellular sodium content, while those acting at the mucosal surface (e.g., amiloride) have the opposite effect (7). Third, the isolated The Journal of Clinical Investigation Volume 53 June 1974-1568-1577epithelial cell preparation allows for evaluation of the effects of agents which influence sodium transport on substrate utilization (7).…”

Section: Introductionmentioning

confidence: 99%

“…ouabain) increase intracellular sodium content, while those acting at the mucosal surface (e.g., amiloride) have the opposite effect (7). Third, the isolated The Journal of Clinical Investigation Volume 53 June 1974-1568-1577epithelial cell preparation allows for evaluation of the effects of agents which influence sodium transport on substrate utilization (7). In the intact toad bladder, transepithelial sodium transport is the major endergonic biologic process and the rate of oxidation of pyruvate closely parallels the rate of active sodium transport.…”

Section: Introductionmentioning

confidence: 99%

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The Effects of the Natriuretic Factor from Uremic Urine on Sodium Transport, Water and Electrolyte Content, and Pyruvate Oxidation by the Isolated Toad Bladder

Kaplan¹,

Bourgoignie²,

Rosecan³

et al. 1974

J. Clin. Invest.

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A B S T R A C T The urine of patients with chronic uremia contains a gel filtration fraction that is natriuretic in the rat. The effects of this fraction on the isolated urinary bladder of the toad were examined in the present studies. When added to the serosal surface of the bladder, a significant and substantial fall in short-circuit current and potential difference was observed. The changes began after a lag period of at least 10 min and continued over a period of 60 min. The decrease in short-circuit current at the end of 1 h averaged 44%. The same fraction from the urine of normal subjects produced no significant change in either short-circuit current or potential difference. When the isolated epithelial cells from the toad bladder were incubated in the presence of the inhibitor, intracellular sodium content increased significantly. There was no change in intracellular water content; hence the intracellular concentration of sodium increased by a mean of 7 meq/liter. The changes in intracellular potassium content and concentration were not statistically significant. When the isolated epithelia were incubated with the uremic factor, there was also a significant decrease in pyruvate utilization in relation to cells from paired hemibladders incubated in the absence of the fraction. The fraction from normal subjects pro- INTRODUCTIONThe effector element of the biologic control system which regulates the renal excretion of sodium is believed to be multifaceted and to have several component parts (1-3). Among these is a postulated natriuretic hormone which theoretically could play a central role in modulating the rate of sodium excretion.In previous studies, we have described an inhibitor of sodium transport in the serum of patients with advanced chronic renal disease (4,5). This serum factor was found to inhibit sodium transport by the isolated frog skin and toad bladder (4) and to produce natriuresis in rats with a reduced nephron population (5). More recently, the same gel filtration fraction obtained from urine of patients with chronic uremia has been found to possess natriuretic activity in the rat (6).In the present studies, attempts have been made to derive information about the site and mechanism of action of the urinary inhibitor using the isolated bladder of the toad. The toad bladder lends itself well to this type of study for several reasons. First, the serum factor inhibits transepithelial sodium transport by the anuran bladder, and the urine factor, if it is the same substance, should have similar inhibitory capabilities. Second, isolated epithelial cells removed from the intact toad bladder have been used recently to investigate the site of action of inhibitors of sodium transport (7). Inhibitors that act at the serosal surface of the epithelia (e.g. ouabain) increase intracellular sodium content, while those acting at the mucosal surface (e.g., amiloride) have the opposite effect (7). Third, the isolated The Journal of Clinical Investigation Volume 53 June 1974-1568-1577 1568 epithelial cell prepa...

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Effect of ADH, aldosterone, ouabain, and amiloride on toad bladder epithelial cells

Cited by 93 publications

References 0 publications

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Intracellular sodium ion activity and sodium transport in rabbit urinary bladder.

Effect of aldosterone on the coupling between H+ transport and glucose oxidation.

The Effects of the Natriuretic Factor from Uremic Urine on Sodium Transport, Water and Electrolyte Content, and Pyruvate Oxidation by the Isolated Toad Bladder

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